The activity of innate immunity is not simply dictated by the presence of an antigen but also by the balance between negative regulatory and immune potentiator pathways. Even in the absence of antigen, innate immunity can ‘inflame’ if negative regulators are absent. This resting state is adaptable and dictated by environmental influences, host genetics and past infection history. A return to homoeostasis post inflammation may therefore not leave the tissue in an identical state to that prior to the inflammatory event. This adaptability makes us all unique and also explains the variable outcome experienced by a diverse population to the same inflammatory stimulus. Using murine models we have identified that influenza virus causes a long-term modification of the lung microenvironment by a de-sensitization to bacterial products and an increase in the myeloid negative regulator CD200R (CD200 receptor). These two events prevent subsequent inflammatory damage while the lung is healing, but also they may predispose to bacterial colonization of the lower respiratory tract should regulatory mechanisms overshoot. In the extreme, this leads to bacterial pneumonia, sepsis and death. A deeper understanding of the consequences arising from innate immune cell alteration during influenza infection and the subsequent development of bacterial complications has important implications for future drug development.
Skip Nav Destination
Article navigation
August 2009
-
Cover Image
Cover Image
- PDF Icon PDF LinkFront Matter
- PDF Icon PDF LinkTable of Contents
Conference Article|
July 22 2009
The innate immune rheostat: influence on lung inflammatory disease and secondary bacterial pneumonia
Tracy Hussell;
Tracy Hussell
1
1Imperial College London, Leukocyte Biology Section, National Heart and lung Institute, Sir Alexander Fleming Building, Exhibition Road, London SW7 2AZ, U.K.
1To whom correspondence should be addressed (email t.hussell@imperial.ac.uk).
Search for other works by this author on:
Mary M. Cavanagh
Mary M. Cavanagh
1Imperial College London, Leukocyte Biology Section, National Heart and lung Institute, Sir Alexander Fleming Building, Exhibition Road, London SW7 2AZ, U.K.
Search for other works by this author on:
Publisher: Portland Press Ltd
Received:
March 04 2009
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem Soc Trans (2009) 37 (4): 811–813.
Article history
Received:
March 04 2009
Citation
Tracy Hussell, Mary M. Cavanagh; The innate immune rheostat: influence on lung inflammatory disease and secondary bacterial pneumonia. Biochem Soc Trans 1 August 2009; 37 (4): 811–813. doi: https://doi.org/10.1042/BST0370811
Download citation file:
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Captcha Validation Error. Please try again.